Furthermore, genetic inhibition of SRPK1 using CRISPR had negligible effects on the clonogenic potential of normal mouse HSPCs despite significant reduction in SRPK1 protein levels (Supplementary Fig. 7f, g), but strongly suppressed primary murine MLL-AF9-driven, but not Npm1c-driven, AML cells (Supplementary Fig. 7h, i). This evidence concerns the gene KMT2A and acute myeloid leukemia.